Randolph Nesse's blog about the challenge of applying evolutionary principles in medicine and elsewhere.

Friday, September 10, 2010

George Williams, 1926-2010

George C. Williams, 1926-2010

George C. Williams died on September 8, 2010 at the age of 84. One of the most important biologists of the 20th century, his influence came not from big grants, flashy talks, magazine articles, or scores of graduate students. Instead, he pursued methodical thinking about important questions and distilled his conclusions into crystal clear prose. His approach was consistent. He would be struck by some apparent contradiction between fact and evolutionary theory, and work on it until a resolution emerged. Senescence, sex, menopause, and vulnerability to disease, all are hard to explain in evolutionary terms. In each case, he thought and thought, eventually coming up with a major contribution.

Instead of marshaling all the evidence for his theory, and disparaging the rest, his work is a model of objectivity. In that article I also argued that he was neither an adaptationist nor an anti-adaptationist; if anything, he was a "maladaptationist." We shared a fascination with aspects of bodies and minds that just didn't seem to make sense in evolutionary terms. Gradually, we figured out ways of providing evolutionary explanations for many such traits. Now, scores of researchers are expanding the field of evolutionary medicine. In typical fashion, he insisted on naming the field "Darwinian medicine," because that term was slightly more accurate, too bad about readers who might better accept a blander designation. He is, and will always be, the father of Darwinian medicine.

Many other commentators will confirm the magnitude of his influence. Here, I want to offer a more personal perspective. His 1957 paper on senescence and antagonistic pleiotropy changed my career. I started trying to figure out senescence in 1968, as a sophomore at Carelton College. It is highly heritable and highly deleterious, so why didn’t natural selection reduce its influence? Days spent paging through volume after paper volume of Index Medicus turned up all kinds of great ideas about aging, but not George’s article. So, I wrote a paper arguing that senescence might have evolved to speed up the evolution of a species. My professors, not having read Williams, 1966, loved it.

In 1983, after I had joined the medical faculty at Michigan, I was spending lots of time with evolutionary biologists. It was clear they had a scientific foundation for understanding behavior that was lacking in psychiatry. Finally I got up my nerve and told them my theory about senescence. They laughed and laughed. Hadn’t I ever read Williams, 1957? Didn’t I know about the problems with group selection? I realized then that a truly excellent medical education had left me fundamentally ignorant about why organisms are the way they are, and why diseases exist. Once I recognized that senescence had at least two potential evolutionary explanations, I wanted to try to explain everything else about the body that seemed suboptimal. Why is obesity so common? Why is the birth canal so narrow? Why hasn't natural selection eliminated the genes that cause schizophrenia?

I started looking for an evolutionary biologist who might want to collaborate on this project. It was my great good fortune that Michigan was at the center of new evolutionary thinking in the 1980s. Richard Alexander and his grad students meet weekly for riveting seminars, and Bill Hamilton and George Williams came by often. Colleagues at Michigan, some of the best and brightest evolutionary biologists you could hope to find, were remarkably patient with my often embarrassingly ignorant questions. When I finally met George, it turned out that he had been thinking along similar lines; he was looking for a physician collaborator. We spent months talking and exchanging notes, trying to find evolutionary explanations for cancer, schizophrenia, and Alzheimer’s disease. The process was frustrating. Finally, in a simple but profound reframing, we recognized that diseases do not have evolutionary explanations. Instead, we turned our focus to aspects of the body that leave us vulnerable to disease. Then we made progress.

Our first major paper came out in 1991 with the grand title, “The Dawn of Darwinian Medicine.” The bravado turned out to be somewhat justified. The field has grown exponentially. We wrote our 1994 book, Why We Get Sick: The New Science of Darwinian Medicine in an engaging style, hoping that people would read it just for fun. That has worked out well.

Hundreds of publications on aspects of evolution and medicine are now available. In 2009, second editions of major edited volumes and a new textbook were published. A web journal, The Evolution and Medicine Review, provides a central information source. The field is healthy and growing, with one exception: medical schools seem to have no way of incorporating yet another basic science into the curriculum, not even something as fundamental as evolutionary biology. This isn't really surprising. There are no evolutionary biologists on medical school faculties to explain what is missing, and few evolutionary biologists bring in the kind of big grants that make medical school deans eager to start new departments. With time, undergraduates now learning about evolution and medicine will become deans. In the meanwhile, things are developing nicely everywhere else.

George was a wonderful collaborator. We wrote the book by sending drafts of chapters back and forth on computer disks. One of us would write a first draft, the other would completely rewrite it. We agreed on a simple method for staying friends. The revising author could make whatever changes seemed sensible, but was not allowed to look back at his earlier draft. After half a dozen iterations for each chapter, we forgot about who came up with what. We argued at length about many issues, allergy, defenses, menopause, senescence, and morality. It was real back and forth, the kind of very productive careful listening and hard arguing that carves away vagueness.

His wife Doris was not only his steady and loving companion, but a vigorous early research collaborator, and my friend as well. Their joint paper in 1957 on the evolution of altruism came close to describing inclusive fitness, but they veered away and relied instead on a variation of group selection. In typical fashion, they explicitly avoided the engaging word "altruism" and instead advocated using the more neutral terms “social donors” and “social non-donors.” As memes, these were non-starters; selfish genes displaced them completely.

Some have described George as a bit curmudgeonly. I loved his directness. He was never trying to manipulate, always trying to understand. If he thought someone was wrong, he felt it was his obligation to talk with them to figure out what was correct. He was always polite, but he didn't pretend to agree just to be congenial. Not everyone liked that.

There was also a private side of George that few know about. For instance, he devoured fiction and history. He wrote a long work of fiction, an Icelandic saga. Eventually biographers will tell us more, but he has made the task challenging. He had the habit of keeping all of his notes and Icelandic. Sush a characteristic quirk.

It was Alzheimer's disease that took him. The irony is nearly unbearable. We spent hours discussing why such a devastating disease should be so extraordinarily common. The obvious answer, of course, is that selection is weak at advanced ages. The alternative hypothesis, while unlikely, also needed consideration. Perhaps some aspect of the mechanism that causes Alzheimer's disease offers some kind of advantage. For decades I have asked neurologist friends for their thoughts about this, without much luck. Then, just a few months ago, an article appeared about beta-amyloid (Soscia, et al., PLoS ONE, 2010) , the substance contained in plaques on the neurons of those with Alzheimer's disease. It turns out to be quite a potent antimicrobial. How George would've loved that! We would have talked for hours about what this means. Are infectious processes involved in Alzheimer's disease? Or is beta-amyloid merely a response to inflammation? Or is it an epiphenomenon? We also would have talked about the failure of drugs intended to disrupt beta-amyloid formation. In publications just last month, they were shown to be worse than useless, they speed the progression of Alzheimer's disease. And yet, in all of reports of the failure of the drug, there was no mention about the new evidence that beta-amyloid might have some useful function. I wish I could talk with George about all of this, and what we can do about it. I do so miss him.

Dr. Nesse: Thank you for this post and for the reference materials. I am working on a psychology class assignment to discuss how an evolutionary perspective might explain Alzheimer's disease. In my online search, I came across references to Nesse and Williams. I ended up here. What a wonderful tribute you have written to your friend and colleague. Sincerely, Jill Elswick

Thank you Dr. Nesse for this tribute. I still recommend "Why We Get Sick" to people regularly and hope that another book can be written in Dr. Williams honor with more of your combined thoughts and theories.

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About

Nothing is more interesting than adaptations shaped by natural selection. Except, possibly, maladaptations that leave us vulnerable to disease. This blog is about the challenge of testing hypotheses about adaptation. Many posts are about Darwinian medicine, psychiatry, emotions and moral capacities.For a more formal journal about evolution and medicine, see The Evolution and Medicine Review.